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作 者:雷德亮[1] 罗学港[1] Peter R. Mouton Donald K. Ingram
机构地区:[1]中南大学湘雅医学院解剖学和神经生物学系,长沙410013 [2]National Institute of Health, Gerontology Research Center, Baltimore, MD, USA
出 处:《神经解剖学杂志》2004年第4期337-342,共6页Chinese Journal of Neuroanatomy
基 金:国家自然科学基金 (No. 3 0 3 40 0 0 3 )资助项目
摘 要:切除 2 0~ 2 4月龄 C5 7BL /6NIA小鼠双侧卵巢 ,随后于颈部皮下植入可持续释放 60 d的含 1.7mgβ-雌二醇 (E2 )或含等剂量胆固醇的安慰剂。用免疫组织化学结合无偏性体视学方法 ,分析小鼠齿状回和海马 CA1区小胶质细胞和星形胶质细胞形态和数量的变化。结果发现 :60 d E2处理老年雌性小鼠不仅可以抑制神经胶质细胞的激活 ,而且可以明显降低小胶质细胞和星形胶质细胞的总数 ;神经胶质细胞在脑内免疫和炎症反应过程中起着非常重要的作用。本实验的结果提示 ,雌激素可能通过调节胶质细胞介导的脑内炎症反应通路 ,发挥其神经保护作用。Immunohistochemistry combined with unbiased stereology was used to analyse the morphological and the total number changes of microglia and astrocytes in hippocamal dentate gyrus and CA1 region. The C57BL/6NIA female mice aged at 20-24 months were used in the present study which received bilateral ovariectomy followed by s.c. placement of 60 d release pellete containing 17 β estradial (E2, 1.7 mg) or placebo (cholesterol) treatment. The results showed that long-term E2 treatment in aged female mice not only inhibited the neuroglia activation, but also significantly lowered the total numbers of microglia cells and astrocytes in dentate gyrus and CA1 region of hippocampus compared with placebo. The neuroglia played an important role in mediating the immunological and inflammatory reaction in the brain. These findings indicate that E2 may provide protection against age and neurodegenerative disease by modulating glia-mediated inflammating pathway.
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